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Control of Renal Function

In This Article

Summary

 

 
 
Causes retention of…
Info
Substance
Mechanism
H2O
Na+
K+
 
Angiotensin-II
Causes massive vasoconstriction. Also causes the release of ADH. Also has its own direct effect on the kidneys activated when there is low BP.
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When the JG apparatus experiences a low BP it release Renin. This activates angiotensinogen to AG-I, which is then activated by ACE to AG-II
Vasopressin (ADH)
Acts on the DCT and causes increased synthesis of water channels, thus increasing water re-absorption. Released by the pituitary in response to low BP
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Doesn’t have a direct effect on Na and K. may cause secondary retention of ions via osmosis, to a small degree. if there is excess ADH, then there will be adilutional hyponatraemia.
Aldosterone
Acts on the PCT where the majority of sodium is reabsorbed, causing synthesis of more sodium channels.
Produced by the adrenal glands in response to angiotensin-II and high potassium levels.
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(↑)
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Excess of aldosterone can cause excessive sodium reabsoprtion, excessive potassium excretion. also, lack of aldosterone has the opposite effect
Also – excess sodium retention can cause alkylosis! This because sodium is retained in exchange for H+ at some channels – thus excess H+ will be excreted
Loop diuretic
e.g. Frusemide
Acts on the thick descending loop of Henle. It prevents the sodium / potassium / chloride channel from functioning, thus these ions remain in the filtrate.
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25% of potassium reabsoprtion is prevented. Highly effective at reducing BP and increasing sodium and water excretion. when the drug is stopped there is rebound sodium retention. Excreted by the kidney. Can cause; renal failure (as a result of massive drop in BP), hyponatraemia, hypokalaemia, chochlear damage, hypocalcaemia, hypomagnesaemia
Thiazide diuretics
e.g. bendroflumethazide
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